Murakami Y, Kato Y, Kabayama Y, Tojo K, Inoue T, Imura H
Endocrinology. 1985 Aug;117(2):787-9. doi: 10.1210/endo-117-2-787.
Intracerebroventricular (icv) injection of gamma-aminobutyric acid (GABA) (10 mumol/rat) resulted in an increase in plasma GH in conscious freely moving rats pretreated with normal rabbit serum (0.5 ml/rat, iv). Rabbit antiserum specific for rat GH-releasing factor (GRF) (0.5 ml/rat, iv) abolished GH release induced by GABA in these animals. Rabbit anti-rat GRF serum also blunted GH release induced by a Met5-enkephalin analog, FK33-824 (10 micrograms/100 g BW, iv) in conscious rats. Considering our previous findings that rat GH release induced by FK33-824 was blunted by GABA antagonists (Endocrinology 103:1033, 1981), these results suggest that GH secretion induced by opioid peptides via GABAergic mechanisms is mediated, at least in part, by hypothalamic GRF in the rat.
向经正常兔血清(0.5毫升/只,静脉注射)预处理的清醒自由活动大鼠脑室内(icv)注射γ-氨基丁酸(GABA)(10微摩尔/只大鼠),可导致血浆生长激素(GH)升高。对大鼠生长激素释放因子(GRF)具有特异性的兔抗血清(0.5毫升/只,静脉注射)可消除这些动物中GABA诱导的GH释放。兔抗大鼠GRF血清也可减弱Met5-脑啡肽类似物FK33-824(10微克/100克体重,静脉注射)在清醒大鼠中诱导的GH释放。鉴于我们之前的研究结果表明,FK33-824诱导的大鼠GH释放可被GABA拮抗剂减弱(《内分泌学》103:1033,1981),这些结果表明,阿片肽通过GABA能机制诱导的GH分泌至少部分是由大鼠下丘脑GRF介导的。